Neonatal Neurology Review - Florida Association of ... Neurology Review.pdf · Neonatal Neurology...

Neonatal Neurology Review Leslie A. Parker, PhD, ARNP, NNP-BC Clinical Assistant Professor University of Florida, Gainesville, FL

The speaker has signed a disclosure form and indicated she has no significant financial interest or relationship with the companies or the manufacturer(s) of any commercial product and/or service that will be discussed as part of this presentation.

Session Summary

This session will provide a general overview of the diagnosis and management of neurologic diseases and conditions to help attendants prepare for certification exams.

Session Objectives

Upon completion of this presentation, the participant will:

understand embryology, physiology and pathophysiology of common neurologic conditions in the newborn;

understand etiology and clinical manifestations of common neurologic conditions in the newborn;

understand the treatment of common neurologic conditions in the newborn.

Test Questions

1. Which of the following is not true of a subgaleal hemorrhage?

a. It occurs in the subaponeurotic space b. It is associated with vacuum extraction deliveries c. It can be life threatening d. Can lead to seizures due to irritation of the nervous system

2. Intraventricular hemorrhages:

a. Occur most commonly in the germinal matrix b. Occur most commonly during the birth process c. Often develops after 1 week of age d. Are easily confused with PVL

3. Severe HIE affects which of the following systems:

a. Heart b. Liver c. Kidneys d. All of the above

B2 FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW

B2: NEUROLOGY REVIEW Page 1 of 41

4. Neonatal seizures:

a. Are always seen on EEG b. Are easily diagnosed clinically c. Often occur as generalized seizures d. Considered a symptom of neurologic dysfunction

5. Which of the following is true of spin bifida occulta?

a. A defect in the vertebral arch b. Often associated with significant spinal cord defects c. Associated with protrusion of membranes d. Associated with Arnold Chiari syndrome

References Bassan, H. (2009). Intracranial hemorrhage in the preterm infant: Understanding it, preventing it. Clinics in

Perinatology, 36: 737.

Brand, C.M. (2006). Part 2 Examining the newborn with an open spinal dysraphism. Advances in Neonatal Care, 6(4): 181.

Brand, C.M. (2007). Part 3 Examining the newborn with closed spinal dysraphism. Advances in Neonatal Care, 7(1): 30.

Jenson, F.E. (2009). Neonatal seizures: An update on mechanisms and management. Clinics in Perinatology, 36: 881.

Laptook, A.R. (2009). Use of therapeutic hypothermia for term infants with hypoxic-ischemic encephalopathy. Pediatric Clinics of North America, 56(3): 601-16.

McCrea, H.J. & Ment, L.R. (2008). The diagnosis, management, and postnatal prevention of intraventricular hemorrhage in the preterm neonate. Clinics in Perinatology, 35(4): 777-92.

Mwaniki, M.K., Atieno, M., Lawn, J.E. & Newton, C.R. (2012). Long-term neurodevelopmental outcomes after intrauterine and neonatal insults: A systematic review. Lancet, 379(9814): 445-52.

Nyquist, P. (2010). Management of acute intracranial and intraventricular hemorrhage. Critical Care Medicine, 38(3): 946.

Parker, L. (2005). Early recognition and treatment of birth trauma: Injuries to the head and face. Advances in Neonatal Care, 5(6): 288-97.

Robinson, S. (2012). Neonatal post hemorrhagic hydrocephalus from prematurity: Pathophysiology and current treatment concepts. Journal of Neurosurgery: Pediatrics, 9(3): 242-58.

Shah, D.K., Boylan, G.B. & Rennie, J.M. (2010). Monitoring of seizures in the newborn. Archives of Disease in Childhood, Fetal and Neonatal Edition, 97(1): F65-9.

Session Outline See presentation handout on the following pages.

FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW


http://www.ncbi.nlm.nih.gov.lp.hscl.ufl.edu/pubmed/19501694?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum



http://www.ncbi.nlm.nih.gov.lp.hscl.ufl.edu/pubmed/22380952

http://www.ncbi.nlm.nih.gov.lp.hscl.ufl.edu/pubmed/22380952

Leslie Parker RNC, PhD, NNP‐BC

University of Florida

Okay, Let’s Get This Thing Going‐ Birth trauma

‐ Neural tube defects

‐ Holoprosencephaly

‐ Hydranencephalyy p y

‐ Microcephaly/hydrocephaly

‐ IVH/PVL

‐ HIE

‐ Seizures

‐ Meningitis

Is There Anything Else We Could Possibly Cover?? Birth Trauma



Caput Succedaneum Accumulation of serum above the periosteum

Bruising and petechia

Due to pressure during labor and delivery

C th t li Crosses the suture lines

Avoid confusion with subgaleal hemorrhage

No treatment necessary

Resolves within 24 to 48 hours

Caput Succedaneum Cephalohematoma

Beneath the periosteum

Develops during the first 24 hours of life

Does not extend across the suture lines

Treatment rarely indicated y

Complete recovery occurring by 3 months

Complications include skull fracture, hyperbilirubinemia and mild anemia



Cephalohematoma

Subgaleal Hemorrhage

Bleeding into the subaponeurotic space

Covers the entire cranial vault

Large enough to hold an infant’s entire blood volume

A i d i h i d d li i Associated with vacuum assisted deliveries

Mortality rate as high as 22%



Subgaleal Hemorrhage Initial symptoms are vague

Generalized scalp edema and ecchymosis

Ballottable

Periorbital and periauricular edema

M t i t May progress to serious symptoms

Diagnosis

Based on clinical symptoms

CT or MRI confirms diagnosis

Treatment

Careful monitoring

Transfusion of blood products

Prognosis





Subarachnoid Hemorrhage The most common intracranial hemorrhage

Bleeding into the subarachnoid space from ruptured vessels

Relatively benign and often asymptomatic

Transient seizure activity on day 2‐3

Abnormal neurologic examination

Generally have an excellent prognosis

Massive hemorrhages occasionally develop



Subdural Hemorrhage Hemorrhage between the dura and the arachnoid

Overstretching of blood vessels during a difficult delivery

Severity ranges from asymptomatic lesions to massive y g y phemorrhage

Presents within the first 12 to 72 hours

Symptoms

Seizures and neurologic changes



Subdural Hemorrhage Diagnosis is either CT or MRI

Treatment Varies depending upon location, extent, and progression

Small hemorrhages require careful assessment

d % f Surgery required in 30‐50% of cases

Prognosis

Depends on the extent and severity

Ranges from complete recovery to rapid deterioration and death

Facial Nerve Palsy Injury to the facial nerve

Diagnosis Drooping mouth Perpetually open eye Ineffective suck and swallowing problems Ineffective suck and swallowing problems Persistent drooling

Treatment – Patching and lubricating eye drops– Initial improvement occurs within days– Full recovery may take weeks to months – Surgical intervention may be necessary

Facial Nerve Palsy Brachial Plexus Injury Injury of the upper brachial plexis from C5 to C8 and T1

Due to lateral traction of the neck

Erb’s palsy

– Upper cervical nerves (C5‐C6)

– Paralysis of the arm and shoulder

– Hand muscles remain intact

– Arm lies adducted, prone and internally rotated



Brachial Plexus Brachial Palsy Injury

Erbs Palsy Brachial Plexus Injury Klumpke’s palsy

– Injury to nerve roots C6 to T1

– Normal upper arm and shoulder movement

– Paralysis of the wrist and hand

Injury to the entire brachial plexus

– Paralysis of the entire upper extremity

– Concurrent sensory loss



Brachial Plexus Injury Treatment Conservative treatment

– Physical therapy

– 30% of brachial plexus injuries completely recover

Surgical intervention Prognosis Prognosis

– Dependent on degree and location of damage– Full spontaneous recovery if some improvement within 2 weeks

– Partial recovery if initial improvement is delayed until 4 to 6 weeks

– Significant permanent deficit if no improvement by 3 months

Craniosynostosis Premature closure of cranial sutures leading to an

abnormally shaped head

Scaphocephaly

Premature closure of the sagittal sutures

Elongates in the occipitofrontal diameter Elongates in the occipitofrontal diameter

Brachycephaly

Premature closure of the coronal sutures

Overgrowth of the vertex and lateral aspects of the head

Cranial Sutures Scaphocephaly



Brachycephaly Craniocynostosis Diagnosis

CT

Palpate for sutural ridge

Treatment Surger to remo e a strip of bone Surgery to remove a strip of bone

Neural Tube Defects Failure of the neural folds to fuse and form the

neural tube

Secondary malformations of the skeletal structure and skin

Wide spectrum of abnormalities Wide spectrum of abnormalities



N l b

Rostral neuropore closing

Forebrain prominence

Heart prominenceRostral neuropore

Neural groove

W.B. Saunders Company items and derived items Copyright (c) 1999 by W.B. Saunders Company

Neural tubeSomites

Connecting stalk

Yolk stalk

A B

Somites

AmnionCaudal neuropore

Caudal neuropore

Spina Bifida Occulta A defect in the vertebral arch

Usually presents as a small dimple with a tuft of hair

Membranes don’t externally protrude

Usually asymptomatic but significant defects of the y y p gspinal cord can occur

Spinal Bifida Occulta Spina Bifida Cystica Protrusion of the spinal cord and/or meninges

through a defect in the arch

May occur anywhere along the vertebral column

Most common in the lumbar region



Spina Bifida Cystica Menigocele (25%)

Sac contains the meninges

Spinal cord in normal position

A dermal covering presentg

Defective axial skeleton

Prognosis

Usually normal

Spinal cord abnormalities are possible

Meningocele

Spina Bifida Cystica Menigomeyelocele (75%)

Sac contains meninges and neural tissue

The spinal cord is a rudimentary neural tube

Clinical manifestations Clinical manifestations

Dependent on the level of the defect

Functional abnormalities are inferior to the defect

69% in the lumbar region

Paralysis

Loss of sensation

Sphincter paralysis

Meningomyelocele



Types of Spina Bifida Arnold‐Chiari Malformation Displacement of the medulla oblongata, the fourth

ventricle and some of the cerebellum into the cervical canal

CSF flow is impaired

Diagnosed by CT or MRI

Arnold Chiari MalformationTreatment

Prone position, sterile wrap, antibiotics

Surgery within 24‐48 hours

Treat hydrocephalus

Multidisciplinary approach

Goal: assist each child to develop maximum function and independence

Family counseling Long term prognosis

Genetic counseling



Prognosis Dependent on the level of the lesion

14% mortality

73% of survivors have IQ >85

87% ambulatory

90% lack bowel and bladder control

Rachischisis Open spinal cord

Failure of neural folds to fuse

Often associated with anencephaly

Rachischisis Congenital Anomalies of the Brain Fairly common due to complex neural

embryology

3:1000



Cranial Meningocele

Contains only the

meninges

Encephalocele

Affects the meninges and part of the brain

60% are occipital

Can be frontonasal, intranasal, nasopharnyx

Diagnosis

Obvious at birth

CT to assess for other brain abnormalities

Treatment

Prognosis

Encephalocele Anencephaly Failure of the rostral neuropore to close

Missing forebrain

Remainder of the brain is degenerative

Absent cranial vault

50% open spinal cord 50% open spinal cord

Stereotypical movements

Spontaneous/pain induced movements

Intact reflexes



Anencephaly

Anencephaly Diagnosis

Obvious at birth

Increased alpha fetoprotein

Prenatal ultrasound

Polyhydramnios

Post term delivery

Supportive treatment

Hydranencephaly Complete or nearly complete absence of the cerebral hemispheres

Intact brain stem

Etiology Severe hydrocephaly Severe hydrocephaly

Inutero infection

Vascular occlusion

Clinical manifestations May appear normal at birth

Irritability/Hyper/hypotonia

Intact reflexes



Hydranencephaly

Prognosis

Usually die early in infancy

No cognitive d ldevelopment

Hydranencephaly

Holoprosencephaly Affect the midfacial region and brain

Failure of the prosencephalon to cleave

Olfactory and optic bulbs

Telencephalon and diencephalon

Wall Cavity

Forebrain(prosencephalon)

Telencephalon

Walls

Cerebralhemispheres

Thalam, etc.

5 Secondaryvesicles

3 Primaryvesicles

Diencephalon


Midbrain

Pons

Cerebellum

Medulla

Spinal cord

Diencephalon

Mesencephalon

Metencephalon

Myelencephalon

Midbrain(mesencephalon)

Hindbrain(rhombencephalon)



Hindbrain Cerebral hemisphere Cerebellum

Midbrain


Forebrain Optic cup Olfactory bulb Optic nerve

A B

Slide 18.18

Holoprosencephaly

Clinical manifestations

Wide spectrum

Single or divided eye in a single orbit

Arhinia (absent nose)

Proboscis (fleshy nose‐like appendage) Proboscis (fleshy nose like appendage)

Alobar brain

Holoprosencephaly



Microcephaly Definition > 2 SD below the mean

Etiology

Small brain = small cranium

Chromosomal abnormalities

TORCH infections

Cerebral atrophy

Perinatal infections

Metabolic causes

Microcephaly Lissencephaly

Near‐total or total absence of cerebral convolutions (agyria)

Pachygyria

few broad gyri and shallow sulci

Lissencephaly



Microcephaly Clinical manifestations

Small or absent anterior fontanel

Round head

Recessed/sloped forehead

l d Mental retardation

Microcephaly

MicrocephalyHydrocephaly

Imbalance between CSF production and absorption

Excessive CSF in the ventricular system

Excess formation of CSF (Choroids plexus tumor)

Decreased absorption of CSF

Ob t ti f fl Obstruction of flow

Dilated ventricles may compress brain tissue



Hydrocephalus Hydrocephalus

Hydrocephalus Communicating

Obstruction occurs after CSF exits the ventricles

Noncommunicating

Obstruction occurs along the passages connecting the t i lventricles

Hydrocephalus Etiology

Aqueductal stenosis

Arnold‐chiari malformation

IVH

Tumor

Infection



Aquaductal Stenosis Hydrocephalus Diagnosis Head circumference

Transillumination

Ultrasound

CT MRI CT or MRI

Treatment – VP shunt Drains CSF from ventricles into peritoneum

Complications Infection

Disconnection

Ventricular Access Device



Periventricular/Intraventricular Hemorrhage

Incidence

Increasing

25 to 30% of VLBW infants

Most common in the first 12 hours

50% by 24 hours

90% by 72 hours

Subependymal Germinal Matrix

Most common area of origination

Beneath the ventricular wall

Produces glial cells and neurons

Most prominent between 24‐32 weeks

Primitive and highly vascular Primitive and highly vascular

Vessels are immature

Lack muscle and collagen

Susceptible to injury



Germinal Matrix

Bleeding into germinal matrix

Hematoma forms

Blood is released into Blood is released into ventricular system if the hematoma ruptures

Intraventricular Hemorrhage Catastrophic

Acute presentation

Rapid and severe

Neurologic and systemic deterioration

Hi h li High mortality

Salutatory Evolves over hours to days

Changes in neurologic status

Silent (50%) No overt deterioration

Classification

Papile’s classification Grade I – bleeding into the germinal matrix

Grade II – rupture into the ventricles without ventricular enlargement g

Grade III – ventricles are completely filled and at least one lateral ventricle is enlarged

Intraventricular Hemorrhage

Volpe’s classification Grade I – bleeding into the germinal matrix

Grade II – blood fills less than 50% of the ventricle

Grade III blood fills over 50% of the ventricle Grade III – blood fills over 50% of the ventricle



Grade I Grade II

Grade III Grade III With Enlarged Ventricles



Grade IV Hemorrhage Hemorrhagic necrosis of the periventricular

white matter

67% unilateral

80% associated with a large IVH

Hemorrhage due to venous infarction from obstructed blood flow

Grade IV IVHGERMINAL MATRIX HEMORRHAGE

PERIVENTRICULAR VENOUS CONGESTION

PERIVENTRICULAR ISCHEMIA

PERIVENTRICULAR HEMORRHAGIC INFARCTION

Grade IV Pathogenesis of IVH

Fluctuating cerebral blood flow

Lack of autoregulation

Pressure‐passive cerebral circulation

Related to prematurity, asphyxia, hypoxia, p y, p y , yp ,hypercapnea

Arterial hypotension

Ischemia, injury and subsequent rupture of the capillary wall



Pathogenesis of IVH Increased venous pressure impedes cerebral venous

return causing venous congestion

Heart failure, PPV, high CPAP, labor and delivery

Excess fibrinolytic activity

Platelet and coagulation disturbances

Inflammatory cytokines

Risk Factors for IVH Prematurity Respiratory distress Pneumothorax Asphyxia SeizuresSeizures Apnea Manipulation (tracheal suctioning, positioning,

handling) Rapid infusion of IV fluids/colloids Clotting disorders Breathing out of sync with the ventilator

Diagnosis Clinical

Decreased hematocrit

Bulging fontanele

Change in level of consciousnessg

Ultrasound

Prognosis Grade I + II

Similar to infants with no IVH

Increased risk for learning problems

Grade III

40% have major disabilities

% h h l d ff l 50% have school difficulties

Grade IV

Mortality is 40%

75% risk of neurologic impairment

CP

Low cognitive scores

Seizures

Visual disturbances



Posthemorrhagic Hydrocephalus

Pathogenesis

Blood clot obstruction

Obstructive inflammation and scarring

Incidence

50% transient venticulomegaly

50% require treatment

Occurs within 4 weeks Monitoring Weekly cranial ultrasound Serial head circumferences

Posthemorrhagic HydrocephalusTreatment

Goals Maintain normal ICP Prevent compression of the periventricular white

matterS b l f Sustain cerebral perfusion

Serial LPs

VP shunts

50% resolve with no treatment

Prenatal Prevention of IVH

Prevention of prematurity

Good luck with this one!

Prenatal transport

Antenatal corticosteriods

Matures blood vessels in the germinal matrix

Decreases incidence by 50%

Postnatal Prevention of IVH Appropriate neonatal resuscitation

Correction/prevention of hemodynamic disturbances

Avoidance of shifts in CBF

Correction of coagulationg

Indomethacin and Ibuprophen Decreases CBF and CBF fluctuations by inhibiting

prostaglandin synthesis

Prostaglandin is important in control of CBF control



Periventricular Leukomalacia Occurs only in premature infants

Incidence

4‐26% of infants < 1500 grams

27‐30 weeks have highest incidence

Ri k f Risk factors

Often associated with an IVH

Evidence of infective component

PROM > 12 hours

Intra‐uterine infection

PROM + chorio = highest incidence

Pathogenesis of PVL Ischemic lesion

Periventricular white matter necrosis Watershed blood supply

High metabolic rate

Small cysts in white matter Small cysts in white matter

Diagnosis Periventricular echodensities on ultrasound

Ultrasound only detects 40‐60%

MRI

Treatment



Prognosis Cerebral palsy

Lower limbs

Developmental delays

Hypoxic Ischemic Encephalopathy

Major cause of acute mortality and chronic neurologic disability

Occurs in both term and preterm infants

10‐15% mortality

40% of survivors have permanent handicaps

Mental retardation

Cerebral palsy

Learning disabilities

Epilepsy

Etiology Placental, fetal or maternal 50% predicted by antenatal/perinatal history

Decreased fetal movement Abnormal NST Abnormal biophysical profile Scalp pH Scalp pH Abnormal FHR MSF Decreased amniotic fluid

Effects of HIE Conversion to anaerobic metabolism

Rapid depletion of ATP

Accumulation of lactic acid

Failure of normal metabolic activity

Intracellular pump function failureA l i f di l i d i b i ll Accumulation of sodium, calcium and water in brain cells

Cellular death

Accumulation of fatty acids and free radicals

Excess release of neurotoxic excitatory neurotransmitters

Cell apoptosis



Phases of HIE Early phase

Decreased brain temperature

Local release of the neurotransmitter GABA

Temporarily decrease cerebral oxygen demand and limit impact

Latent phase Intervention may be effective

Secondary phase of Injury

Apoptosis – programmed cell death

Sarnat Stages A clinical staging tool for HIE

Developed for use in full term infants

Provides information for optimal medical management g

Predicts neurologic prognosis

Sarnat Stages Clinical Manifestations

Depends on severity, timing and duration

Seizures 50‐70%

First 24 hours

E li h i di Earlier the seizure = more severe disease

May be refractory

Abnormal respiration

Abnormal positioning/tone

Irritability



Clinical Manifestations

Impaired glucose delivery and metabolism

Anaerobic metabolism

Renal failure

Myocardial dysfunction Myocardial dysfunction

Decreased cardiac output

Clinical Manifestations Pulmonary involvement

PPHN

Pulmonary edema

Respiratory depression

P l h h Pulmonary hemorrhage

Surfactant inactivation

Clinical Manifestations Liver

Impaired liver function

Clotting disorders

GI Changes in GI motilityg y

Mucosal damage

NEC

Heme DIC

Decreased clotting factors

Thrombocytopenia

Brain Imaging Early (2‐4 days)

Cerebral edema

Decreased tissue attenuation

Late (2‐4 weeks)

Encephalomalacia

Cerebral atrophy



Early CT Encephalomalacia

Management Delivery room resuscitation

Maintain ventilation

Maintain oxygenation

Maintain perfusion Maintain perfusion

Correction of acidosis

Inhibits surfactant production

Increases pulmonary vascular resistance

Reduces myocardial contractility

Management Monitor for renal impairment

Treat DIC

Monitor electrolytes

Maintain normal metabolic state

May require 9‐15 meq/kg/min glucose

Increased calcium requirements



Management Control seizures

Control cerebral edema

Fluid restriction

Hyperventilation

Diuretics

Withdrawal of treatment

Hypothermia

Insult Primary Neuronal Death

Opportunity for Opportunity for Neuronal Rescue

Delayed Neuronal Death

Hypothermia Evidence is compelling

Effective in mild to moderate HIE

Decreases rate of cellular death

D ll l b li Decreases cellular metabolism

Conserves ATP stores

Limits free radical release

Hypothermia Criteria vary among institutions

Initiate less than 6 hours after insult

Continue for 48‐72 hours

Cool to approximately 34‐35 degrees

Rewarm over 12‐24 hours

Complications Decreased heart rate, cardiac output and stroke

volume

Renal impairment

Acid‐base and electrolyte abnormalities

Coagulation abnormalities



Prognosis Indicators of poor outcome

Apgars less than 3 at 10 minutes Early onset and/or refractory seizures Abnormal neurologic signs at discharge Persistently abnormal CT Markedly abnormal EEG or an abnormal EEG after 3 Markedly abnormal EEG or an abnormal EEG after 3

days

Indicators of normal outcome

Normal neuro exam within the first week

Normal EEG within 3 days

Neonatal Seizures Symptom of neurologic dysfunction

Excessive simultaneous electrical discharge or depolarization

Excessive excitatory amino acid release

fi i i hibi i (i GA A) Deficient inhibitory neurotransmitters (ie GABA)

Critical to recognize, determine etiology and treat

May represent significant illness needing treatment

Interference with supportive measures

Can cause brain injury

Etiology of Seizures HIE

Most common cause

Subtle, multifocal clonic or focal clonic

Intracranial/intraventricular hemorrhage

Subarachnoid hemorrhage

Subdural hemorrhage

Arterial or venous stroke



Etiology of Seizures Metabolic disturbance

Hypoglycemia

Hypocalcemia

Hyponatremia

Hypernatremia Hypernatremia

Inborn errors of metabolism

Etiology of Seizures Intracranial Infection

Bacterial

Toxoplasmosis

CMV

Herpes

Developmental Defects

Migrational abnormalities

Cerebral cortical dysgenesis

Drug withdrawal

Etiology of Seizures Benign familial neonatal seizures

First 48‐72 hours

Positive family history

Normal development

Benign idiopathic neonatal seizures

Fifth‐day fits

Day 4‐6

Normal development

Classification of Seizures Subtle

Ocular phenomena Horizontal deviation +/‐ jerking of eyes Sustained eye opening with ocular fixation

O l b l li l Oral‐buccal‐lingual movements Rowing of arms or pedaling Autonomic changes



Classification of Seizures Clonic Rhythmic Slow (1‐3 jerks/sec)

Focal clonicF d/ l i i id Face, upper and/or lower extremities on 1 side

OR Axial structures (neck or trunk) on one side

Multifocal clonic Several body parts in a migrating fashion Seen in term infants

Classification of Seizures Classic Generalized clonic seizures

Bilateral symmetric and synchronous movements

Rare in neonate

Diagnosis HISTORY, HISTORY, HISTORY

Electrolytes

Sepsis workup including LP

Ultrasound/CTUltrasound/CT

EEG

80% of neonatal seizures are not seen on EEG

Electrical seizures may not correlate with clinical seizures

Video EEG

aEEG

Treatment Treat underlying etiology

Medications

Phenobarbitol

Phosphyntoin

Benzodiazepines



Prognosis

Prognosis and etiology are interdependent

Controlling seizures improves outcome

Sequelae include Developmental delays

Motor deficits

Persistent seizures

Meningitis Inflammation of the membranes lining the brain

and the spinal column

Dura mater, pia mater, arachnoid

Purulent exudate covering the meninges and ventricles ventricles



Clinical Presentation Nonspecific symptoms of infection

Irritability

Lethargy

Increased ICP (bulging fontanele, HTN, tremors)( g g , , )

Persistent and severe vomiting

Seizures (20‐50%)

Diagnosis Who do we tap? – controversial

Abnormal CSF findings

> 30 wbc (> 60% PMNs)

Glucose (50% serum)

Protein >100 mg/dl Protein >100 mg/dl

Positive culture/gram stain

Treatment and Prognosis 2‐3 weeks of antibiotics

Repeat CSF studies until sterile

Prognosis 20‐50% have permanent sequlae

Hearing/speech difficulties Hearing/speech difficulties

Hydrocephaly

Blindness

Seizures

Mental retardation

Cerebral palsy

The End

Questions?



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